Supporting this conclusion is the observation that depletion of TGF-β signaling in γδT IELs leads to increased susceptibility to and exacerbation of DSS-induced colitis, as evidenced in both Smad3−/− mice and γδT cell-specific TGF-β receptor I-deficient mice, due to enhanced bacterial invasion and damage to the epithelial barrier resulting from the reduction of γδ IELs in these knockout mice. This evidence concerns the gene SMAD3 and colitis.